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Figure 5 | Skeletal Muscle

Figure 5

From: STIM1 as a key regulator for Ca2+ homeostasis in skeletal-muscle development and function

Figure 5

Gene expression involved in Ca2+and/or contractility. Plots represent gene expression in quadriceps skeletal-muscle samples of controls (CTL, n = 10-12) and patients with Duchenne muscular dystrophy (DMD, n = 10 - 12) in arbitrary units (A.U.). Data were obtained from GEO reference series GSE1007 (STIM1, STIM2, ORAI1, ITPR1 and CASQ1) and GSE1004 (TRPC1, ATP2A1, RYR1 and MYH2) [116118] comparing the mRNA-expression levels in normal and dystrophic patients (http://www.ncbi.nlm.nih.gov/geo/). Graphs represent box plots, indicating the mean (square symbol), the median (line), the 25th and 75th percentiles (bottom and top of the box), and the 5th and 95th percentiles (whisker range). Strikingly, STIM1-, SERCA1-, RyR1-mRNA levels tended to decline, while STIM2-, TRPC1- and IP3R1-mRNA levels tended to increase. Orai1-, calsequestrin-1- and myosin heavy chain-2-mRNA levels did not significantly alter. This seems opposite to what has been observed in mouse models for Duchenne muscular dystrophy, which displayed excessive Ca2+ influx and up-regulation of STIM1/Orai1 [106]. In human patients suffering from Duchenne muscular dystrophy, TRPC1 elevations may account for the increase in Ca2+ influx, leading to Ca2+-dependent apoptosis and muscle degeneration. This indicates that caution should be taken from extrapolating results from mouse models for pathophysiological conditions to human pathophysiological conditions. Abbreviations indicate the gene names for stromal interaction molecule 1 (STIM1), stromal interaction molecule 2 (STIM2), Orai1 (ORAI1), canonical transient receptor potential 1 (TRPC1), sarcoplasmic/endoplasmic-reticulum Ca2+-ATPase 1 (ATP2A1), ryanodine receptor 1 (RYR1), inositol 1,4,5-trisphosphate receptor 1 (ITPR1), calsequestrin 1 (CASQ1), and myosin heavy chain IIa (MYH2).

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